Through upregulating IGF-1R and c-KIT to affect the cell viability, proliferation, and apoptosis of imatinib treated GIST cells, downregulation of lncRNA CCDC26 promoted the process of imatinib resistance which could be used to develop potential strategies overcoming the imatinib resistance of GIST patients (Cao K. et al., 2018; Yan et al., 2019b). The gene discussed is KIT; the disease is gastrointestinal stromal tumor.